38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses

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1 Chapter 1: Exam Structure, Blueprint & Clinical Decision-Making

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7 Chapter 7: Pediatric Health Maintenance & Surveillance

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8 Chapter 8: Behavioral Health & Safety Screening

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12 Chapter 12: Sexual Health, Infectious Disease Screening & Contraception

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17 Chapter 17: Neurologic Emergencies: Stroke & Altered Consciousness

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18 Chapter 18: Neurologic Trauma & Acute Cranial Emergencies

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19 Chapter 19: Acute Abdominal, Pelvic & Gastrointestinal Emergencies

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20 Chapter 20: Acute Pulmonary & Airway Emergencies

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21 Chapter 21: Acute Traumatic Injuries & Wound Care

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22 Chapter 22: Acute Orthopedic & Musculoskeletal Emergencies

22.1 Acute Ambulatory Fractures & Initial Splinting 22.2 Compartment Syndrome & Major Orthopedic Trauma 22.3 Septic Arthritis & Acute Microcrystalline Crises

23 Chapter 23: Severe Infections, Sepsis & Systemic Emergencies

23.1 Sepsis, Septic Shock & Initial Fluid Resuscitation 23.2 Necrotizing Soft Tissue Infections & Severe CNS Infections 23.3 Anaphylaxis Diagnosis, Epinephrine Dosing & Airway Protection

24 Chapter 24: Metabolic, Endocrine & Electrolyte Emergencies

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25 Chapter 25: Hematologic, Urologic & Dental Emergencies

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26 Chapter 26: Psychiatric, Behavioral & Obstetric/Gynecologic Emergencies

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27 Chapter 27: Acute Head, Neck & Neurologic Symptoms

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28 Chapter 28: Acute Cranial Nerves, Hearing & Sensory Symptoms

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29 Chapter 29: Acute Upper Respiratory Tract Infections

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30 Chapter 30: Acute Lower Respiratory Infections & Cough

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33 Chapter 33: Acute Upper Gastrointestinal Conditions

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34 Chapter 34: Acute Lower Gastrointestinal Conditions

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35 Chapter 35: Inflammatory, Functional & Malabsorptive GI Disorders

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36 Chapter 36: Acute Abdominal, Hepatic & Biliary Disorders

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37 Chapter 37: Acute Abdominal Wall, Hernias & Dental Conditions

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38 Chapter 38: Acute Infectious Dermatoses

38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses 38.2 Fungal Skin Infections: Tinea Corporis, Cruris, Pedis & Onychomycosis 38.3 Viral Cutaneous Infections: Herpes Simplex, Zoster & Molluscum Contagiosum

39 Chapter 39: Inflammatory, Allergic & Autoimmune Dermatoses

39.1 Atopic Dermatitis, Contact Dermatitis & Eczematous Flares 39.2 Non-Infectious Rashes: Urticaria, Drug Eruptions & Erythema Multiforme 39.3 Cutaneous Malignancies & Premalignant Lesions: AK, BCC, SCC & Melanoma

40 Chapter 40: Acute Shoulder, Elbow & Upper Extremity Injuries

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41 Chapter 41: Acute Knee, Ankle & Lower Extremity Injuries

41.1 Meniscal Tears, Ligamentous Knee Injuries & Patellofemoral Pain 41.2 Ankle Sprains, Ottawa Ankle Rules & Achilles Tendinopathy 41.3 Plantar Fasciitis, Shin Splints & Overuse Syndromes

42 Chapter 42: Acute Ambulatory Fractures & Dislocations

42.1 Distal Radius, Scaphoid & Common Upper Extremity Fractures 42.2 Metatarsal, Clavicle & Common Lower Extremity Fractures 42.3 Joint Dislocation Management: Nursemaid's Elbow & Shoulder Subluxation

43 Chapter 43: Acute Axial Musculoskeletal Pain & Falls

43.1 Acute Low Back Pain: Red Flags, Strain & Disc Herniation 43.2 Acute Cervical Strain, Whiplash & Axial Neck Pain 43.3 Evaluation of Falls in Ambulatory & Older Patients

44 Chapter 44: Acute Inflammatory Arthropathies & Generalized Pain

44.1 Acute Inflammatory Arthritis & Spondyloarthropathies 44.2 Myalgias, Rhabdomyolysis & Post-Viral Pain Syndromes 44.3 Acute Non-Headache Pain Management Strategies

45 Chapter 45: Acute Renal, Urinary & Genitourinary Conditions

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46 Chapter 46: Acute Male Genitourinary & Prostatic Conditions

46.1 Acute Prostatitis, Epididymitis & Orchitis 46.2 Acute Scrotal Pain: Torsion vs Appendage, BPH & Male Genital Emergencies 46.3 Acute Urinary Retention & Incontinence Evaluation

47 Chapter 47: Acute Women's Health & Early Pregnancy Care

47.1 Early Pregnancy Diagnosis, Dating & Initial Complications 47.2 Abnormal Uterine Bleeding & Acute Menstrual Disorders 47.3 Premenstrual Syndrome & Premenstrual Dysphoric Disorder

48 Chapter 48: Breast Disorders, STIs & Pediatric Elimination

48.1 Palpable Breast Mass, Mastitis & Nipple Discharge 48.2 Sexually Transmitted Infections: Diagnosis, Staging & CDC Guidelines 48.3 Pediatric Enuresis & Encopresis

49 Chapter 49: Systemic Signs, Metabolic Dysregulation & Miscellaneous Infections

49.1 Acute Fever, Sepsis Screening & FUO in Primary Care 49.2 Acute Hyperglycemia & Symptomatic Hypoglycemia 49.3 Electrolyte Abnormalities: Mild-to-Moderate Disturbances 49.4 Vector-Borne, Tick-Borne & Rickettsial Illnesses

50 Chapter 50: Chronic Cardiovascular Diseases: Hypertension & Ischemia

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51 Chapter 51: Chronic Vascular, Valvular & Dyslipidemic Diseases

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52 Chapter 52: Chronic Respiratory Diseases: Asthma & COPD

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53 Chapter 53: Chronic Metabolic Diseases: Diabetes Mellitus

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54 Chapter 54: Obesity, Nutrition & Metabolic Bone Diseases

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55 Chapter 55: Chronic Endocrine Disorders

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56 Chapter 56: Chronic Kidney Disease & Venous Disorders

56.1 Chronic Kidney Disease: KDIGO Staging & Renoprotective Therapy 56.2 Chronic Venous Insufficiency, Stasis Dermatitis & Lymphedema 56.3 Chronic Electrolyte & Acid-Base Management in CKD

57 Chapter 57: Chronic Gastrointestinal & Hepatic Diseases

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58 Chapter 58: Colorectal Surveillance & Chronic Pancreaticobiliary Care

58.1 Post-Polypectomy Colorectal Polyp Surveillance Guidelines 58.2 Chronic Pancreatitis & Exocrine Pancreatic Insufficiency 58.3 Chronic Nausea, Gastroparesis & Functional GI Disorders

59 Chapter 59: Chronic Musculoskeletal & Rheumatologic Disorders

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60 Chapter 60: Chronic Neurologic & Neurodegenerative Disorders

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61 Chapter 61: Chronic Peripheral Nerves, Pain & Sensory Disorders

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62 Chapter 62: Chronic Psychiatric Disorders

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63 Chapter 63: Chronic Behavioral Health & Neurodevelopmental Conditions

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64 Chapter 64: Chronic Substance Use Disorders & Tobacco Cessation

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65 Chapter 65: Chronic Dermatologic Conditions

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66 Chapter 66: Chronic Reproductive, Infectious & Geriatric Special Care

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67 Chapter 67: Continuity Care: Sleep, Fatigue, Cancer, Pregnancy & the Adult Preventive Visit

67.1 Chronic Insomnia & Obstructive Sleep Apnea 67.2 Chronic Malaise, Fatigue & ME/CFS 67.3 Primary Care During Cancer Treatment & Survivorship 67.4 Routine Prenatal Care & Longitudinal Pregnancy Management 67.5 The Periodic Adult Health Examination & Medicare Annual Wellness Visit

38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses

Key Takeaways Explain This Topic AI

Non-bullous impetigo presents with classic honey-colored (meliceric) crusts caused by Staphylococcus aureus and Streptococcus pyogenes; localized disease (<3-5 lesions without systemic symptoms) responds to topical mupirocin 2% or retapamulin 1% ointment for 5 days, whereas widespread lesions or ecthyma mandate oral cephalexin or dicloxacillin.

Bullous impetigo is caused exclusively by S. aureus producing exfoliative toxin A, which cleaves desmoglein-1 in the superficial epidermis (stratum granulosum) to produce flaccid fluid-filled bullae that rupture into collarettes of scale, requiring systemic oral beta-lactam therapy.

Erysipelas involves the upper dermis and superficial lymphatics (predominantly Group A Streptococcus) presenting with fiery red, raised, sharply demarcated borders and rapid systemic toxicity, whereas non-purulent cellulitis involves deeper dermis and subcutaneous fat with flat, poorly demarcated spreading erythema treated with oral cephalexin 500 mg QID for 5-7 days.

Incision and drainage (I&D) is the primary definitive therapy for simple abscesses without routine antibiotics; adjunctive oral antibiotics (TMP-SMX, doxycycline, or clindamycin) are indicated only for cellulitis >2 cm, systemic signs (T >38°C, HR >90), multiple collections, immunosuppression, facial danger triangle, or drainage failure.

Empiric outpatient oral regimens for CA-MRSA include trimethoprim-sulfamethoxazole (TMP-SMX 1-2 DS tablets BID), doxycycline (100 mg BID), or clindamycin (300-450 mg TID, pending D-test); recurrent furunculosis is managed with mupirocin nasal ointment BID for 5 days plus chlorhexidine body washes.

Last updated: September 2026

Spectrum of Bacterial Skin & Soft Tissue Infections

Bacterial skin and soft tissue infections (SSTIs) constitute one of the most frequent reasons for acute outpatient visits and hospital admissions in primary care. Accurate management requires clinicians to systematically distinguish superficial epidermal infections from deep dermal and subcutaneous processes, recognize surgical emergencies such as necrotizing fasciitis, and apply rigorous antimicrobial stewardship to avoid overprescribing antibiotics for uncomplicated drained abscesses while providing timely coverage for community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and Streptococcus pyogenes (Group A Streptococcus [GAS]). ANATOMICAL DEPTH OF BACTERIAL CUTANEOUS INFECTIONS

• Skin Layer Pathology Dominant Pathogens
• ─────────────────────────────────────────────────────────────────────────────
• Epidermis (Subcorneal) Impetigo (Non-bullous/Bullous) S. aureus, S. pyogenes
• ─────────────────────────────────────────────────────────────────────────────
• Deep Epidermis/Dermis Ecthyma (Ulcerative impetigo) S. pyogenes, S. aureus
• ─────────────────────────────────────────────────────────────────────────────
• Upper Dermis & Erysipelas S. pyogenes (GAS)
• Superficial Lymphatics (Sharply demarcated, raised)
• ─────────────────────────────────────────────────────────────────────────────
• Deep Dermis & Non-Purulent Cellulitis GAS, Groups B/C/G Strep,
• Subcutaneous Fat (Poorly demarcated, flat) MSSA
• ─────────────────────────────────────────────────────────────────────────────
• Hair Follicle & Dermis Folliculitis / Furuncle / CA-MRSA, MSSA
• Carbuncle / Cutaneous Abscess
• ─────────────────────────────────────────────────────────────────────────────
• Deep Fascia & Muscle Necrotizing Fasciitis Polymicrobial (Type I)
• (SURGICAL EMERGENCY!) GAS monomicrobial (Type II)
• Impetigo & Ecthyma

Impetigo is a highly contagious, superficial bacterial infection of the epidermis, occurring predominantly in children aged 2 to 5 years, though individuals of any age can be affected in warm, humid conditions or settings of close physical contact (e.g., daycare centers, sports teams).

1. Non-Bullous Impetigo

Epidemiology & Etiology : Accounts for approximately 70% of all impetigo cases . The primary causative organisms are Staphylococcus aureus (most common) and Streptococcus pyogenes (Group A beta-hemolytic Streptococcus [GAS]), either alone or in combination.

Pathogenesis : Bacteria inoculate through microscopic breaks in the epidermal stratum corneum caused by minor abrasions, insect bites, varicella lesions, or atopic dermatitis. Autoinoculation occurs rapidly via scratching and fingers.

Clinical Presentation :

Initial lesions are transient, thin-walled microvesicles or pustules that rapidly rupture.

The hallmark physical exam finding is superficial, moist erosions covered by thick, adherent, golden, honey-colored ("meliceric") crusts .

Lesions characteristically cluster on the face, particularly around the nares and perioral region , as well as exposed extremities.

Pruritus is common, but systemic symptoms (fever, malaise, toxicity) and marked regional lymphadenopathy are typically absent in mild-to-moderate disease.

Complications : Untreated streptococcal impetigo can precipitate post-streptococcal glomerulonephritis (PSGN) , which typically develops 3 to 6 weeks after cutaneous infection. Crucial Board Pearl : Antimicrobial treatment of impetigo prevents secondary transmission and heals cutaneous lesions, but does NOT prevent the development of post-streptococcal glomerulonephritis ! In contrast to pharyngeal GAS infections, cutaneous GAS infections are not associated with acute rheumatic fever.

2. Bullous Impetigo

Epidemiology & Etiology : Accounts for approximately 30% of impetigo cases , occurring most commonly in neonates, infants, and young children. It is caused exclusively by toxin-producing strains of Staphylococcus aureus .

Pathogenesis : S. aureus produces exfoliative toxin A (ETA), a serine protease that specifically targets and cleaves desmoglein-1 , a key desmosomal cell-cell adhesion protein located exclusively in the superficial epidermis (stratum granulosum). Cleavage of desmoglein-1 results in intraepidermal acantholysis, blistering, and bullae formation without inflammatory cellular infiltrate.

Clinical Presentation :

Begins as small vesicles that enlarge rapidly to form large, flaccid, clear-to-turbid fluid-filled bullae (1 to 2 cm in diameter) on previously intact skin of the trunk, intertriginous folds, face, or buttocks.

Because the blister roof is thin superficial epidermis, the bullae easily rupture, leaving shiny, red, moist, shallow erosions surrounded by a characteristic thin, delicate rim or "collarette" of scale .

In contrast to non-bullous impetigo, honey-colored crusting is minimal or absent.

Bullous impetigo represents a localized manifestation of the same exfoliative toxin responsible for generalized Staphylococcal Scalded Skin Syndrome (SSSS) in neonates and young infants with immature renal toxin clearance.

3. Ecthyma

Pathogenesis & Depth : Ecthyma represents an ulcerative, deeper variant of impetigo that penetrates through the full-thickness epidermis and extends into the deep dermis .

Etiology : Caused predominantly by Streptococcus pyogenes , frequently with secondary S. aureus superinfection. Predisposing factors include poor hygiene, malnutrition, tropical climates, excoriations, homeless populations, and immunocompromised states.

Clinical Presentation :

Presents as painful, "punched-out" round or oval deep cutaneous ulcers with raised, indurated, violaceous borders.

The ulcers are covered by a thick, hard, tightly adherent, yellowish-black crust or eschar.

Removal of the crust reveals a raw, purulent, granulating ulcer base.

Lesions occur most commonly on the lower extremities (shins, dorsum of feet).

Because the dermal basement membrane and papillary dermis are breached, ecthyma heals slowly and invariably resolves with permanent scar formation .

Evidence-Based Treatment Algorithm for Impetigo & Ecthyma

Impetigo Variant Extent / Severity First-Line Antimicrobial Therapy Alternative Regimens (e.g., Penicillin Allergy / MRSA)

Localized Non-Bullous Impetigo Limited lesions (<3-5 discrete lesions), intact overall skin, no systemic symptoms Topical Mupirocin 2% ointment/cream applied TID for 5 days OR Topical Retapamulin 1% ointment applied BID for 5 days Topical Ozenoxacin 1% cream applied BID for 5 days (approved ≥2 months of age)

Widespread Non-Bullous Impetigo Extensive lesions, multiple body sites, scalp involvement, or daycare/sports outbreaks Oral Cephalexin 500 mg PO QID (adults) or 25-50 mg/kg/day divided QID (children) for 5-7 days OR Oral Dicloxacillin 500 mg PO QID for 5-7 days Oral Clindamycin 300 mg PO TID (if suspected MRSA or severe penicillin allergy) OR Amoxicillin-clavulanate 875/125 mg PO BID

Bullous Impetigo Flaccid bullae, multiple lesions (toxin-mediated S. aureus ) Oral Cephalexin 500 mg PO QID (children: 25-50 mg/kg/day divided QID) for 5-7 days OR Oral Dicloxacillin 500 mg PO QID for 5-7 days Oral Trimethoprim-sulfamethoxazole (TMP-SMX) or Oral Clindamycin (if community MRSA prevalence is high)

Ecthyma Deep punched-out dermal ulcers; risk of scar formation Oral Cephalexin 500 mg PO QID for 7-10 days OR Oral Dicloxacillin 500 mg PO QID for 7-10 days Oral Clindamycin 300-450 mg PO TID or TMP-SMX 1-2 DS tablets PO BID (if MRSA suspected)

Tip

PEDIATRIC IMPETIGO PEARL : For mild, localized non-bullous impetigo involving only a few crusted lesions around the nose and mouth, topical mupirocin 2% ointment is equal in clinical efficacy to oral cephalexin, avoids systemic adverse effects (such as gastrointestinal upset and diarrhea), and minimizes selective pressure for broad antimicrobial resistance. Crusts should be gently soaked with warm soapy water before ointment application to facilitate topical penetration.

Cellulitis vs. Erysipelas

Differentiating erysipelas from non-purulent cellulitis is a classic clinical challenge in primary care. Although both represent acute spreading bacterial infections of the skin, their anatomical depth, microbiology, and physical features differ substantially. ERYSIPELAS vs. NON-PURULENT CELLULITIS

• Feature ERYSIPELAS NON-PURULENT CELLULITIS
• ─────────────────────────────────────────────────────────────────────────────
• Anatomic Depth Upper dermis & superficial Deep dermis & subcutaneous
• lymphatics fat
• ─────────────────────────────────────────────────────────────────────────────
• Primary Etiology Streptococcus pyogenes Beta-hemolytic Strep (GAS,
• (GAS >90%) GBS, GCS, GGS) & MSSA
• ─────────────────────────────────────────────────────────────────────────────
• Onset & Toxicity Acute, abrupt onset; Subacute onset (over days);
• high fever, shaking chills mild-moderate systemic signs
• ─────────────────────────────────────────────────────────────────────────────
• Clinical Appearance Fiery bright red, shiny, Dull pink-red, flat, poorly
• indurated, raised border demarcated, ill-defined
• SHARPLY DEMARCATED edges blend into normal skin
• ─────────────────────────────────────────────────────────────────────────────
• Classic Locations Lower extremities, Face Lower leg (unilateral),
• (malar butterfly rash) extremities, abdominal wall
• ─────────────────────────────────────────────────────────────────────────────
• Initial Outpatient Rx Oral Penicillin VK or Oral Cephalexin 500 mg QID
• Amoxicillin or Cephalexin or Cefadroxil 500 mg-1 g daily
• 1. Erysipelas

Pathogenesis & Depth : Involves the upper papillary dermis and superficial cutaneous lymphatics . The superficial anatomical localization accounts for the intense dermal edema, prominent lymphangitis, and conspicuous clinical demarcation.

Etiology : Overwhelmingly caused by Group A beta-hemolytic Streptococcus ( Streptococcus pyogenes ) ; rarely caused by Group B, C, or G streptococci.

Clinical Presentation :

Rapid, dramatic, explosive onset over a few hours.

High fever (often ≥38.5°C to 39.5°C), rigor, tachycardia, and prominent systemic toxicity preceding the skin changes by several hours.

Physical Findings : An area of bright, fiery red, shiny, hot, tense, indurated plaque with a raised, sharply demarcated, elevated advancing border that is palpably distinct from surrounding healthy skin.

Superficial skin involvement may produce an "orange peel" ( peau d'orange ) appearance due to cutaneous lymphatic obstruction surrounding hair follicles.

Locations : Lower extremities are most common (~80%), followed by the face (~15-20%). Facial erysipelas classically presents with a bilateral butterfly-shaped malar distribution, but characteristically spares the nasolabial folds (involvement of the nasolabial folds suggests seborrheic dermatitis or contact dermatitis rather than erysipelas).

First-Line Therapy :

Mild Outpatient Erysipelas : Oral Penicillin VK 500 mg PO QID, Oral Amoxicillin 500 mg PO TID, or Oral Cephalexin 500 mg PO QID for 5 days (extend to 7-10 days if clinical response is slow).

Severe / Toxic / Hospitalized Patients : Intravenous Cefazolin 1 g to 2 g IV every 8 hours or IV Aqueous Penicillin G 2 to 4 million units IV every 4 to 6 hours.

Penicillin-Allergic : Oral Clindamycin 300 to 450 mg PO TID.

2. Non-Purulent Cellulitis

Pathogenesis & Depth : Involves the deeper reticular dermis and subcutaneous adipose tissue .

Etiology : Primarily caused by beta-hemolytic streptococci ( S. pyogenes , Group B S. agalactiae , Group C, and Group G streptococci) in >75% of cases, followed by methicillin-susceptible Staphylococcus aureus (MSSA). Methicillin-resistant S. aureus (MRSA) is an infrequent cause of typical non-purulent cellulitis in the absence of penetrating trauma, purulent drainage, or systemic risk factors.

Clinical Presentation :

Subacute onset progressing over several days.

Localized cardinal signs of inflammation: erythema, warmth, edema, and tenderness .

In contrast to erysipelas, the erythema is flat and poorly demarcated , with indistinct, ill-defined margins that gradually merge into adjacent normal skin.

Fever and systemic toxicity may be present but are generally less acute and dramatic than in erysipelas.

Predisposing Risk Factors : Tinea pedis (especially interdigital maceration serving as the microscopic portal of bacterial entry), chronic venous insufficiency, lymphedema, obesity (BMI ≥30), prior saphenous vein harvest for coronary bypass, and prior episodes of cellulitis.

Diagnostic Stewardship :

Uncomplicated cellulitis is a clinical diagnosis .

Swabbing intact, non-broken skin or sending superficial skin cultures is useless and clinically misleading (grows colonizing skin flora).

Blood cultures are positive in <5% of immunocompetent outpatients and are not recommended for routine, uncomplicated cellulitis.

Blood cultures are indicated ONLY in patients with systemic toxicity, underlying immunosuppression, hematologic malignancy, animal bites, water immersion injuries, or failure to respond to initial empiric therapy.

Marking the border : The leading edge of erythema should be outlined with a surgical skin marker to track clinical response.

Treatment of Typical Non-Purulent Cellulitis :

First-Line Oral Outpatient Therapy : Targets beta-hemolytic streptococci and MSSA:

• Oral Cephalexin 500 mg PO QID for 5 to 7 days ;
• Oral Cefadroxil 500 mg to 1 g PO daily or divided BID for 5 to 7 days;

Oral Dicloxacillin 500 mg PO QID for 5 to 7 days.

Penicillin/Cephalosporin Allergy (non-severe): Oral Clindamycin 300 to 450 mg PO TID.

Duration of Therapy : High-quality randomized controlled trials confirm that 5 to 6 days of oral therapy is just as effective as 10 to 14 days for uncomplicated cellulitis that has shown clinical improvement by day 5. Prolonged antibiotic courses increase adverse drug events and C. difficile colitis without reducing treatment failure.

Non-Pharmacologic Adjuncts : Elevation of the affected extremity above the level of the heart is critical to promote lymphatic and venous drainage, accelerating clinical resolution. Interdigital tinea pedis must be actively identified and treated with topical antifungals to eliminate the primary portal of bacterial entry and prevent cellulitis recurrence.

Clinical Mimics & Red Flags: Recognizing Necrotizing Fasciitis CELLULITIS vs. CLINICAL MIMICS

• Diagnosis Distinguishing Physical & Clinical Characteristics
• ─────────────────────────────────────────────────────────────────────────────
• Venous Stasis BILATERAL lower leg involvement, chronic pitting edema,
• Dermatitis hemosiderin brown pigmentation, lipodermatosclerosis
• ("inverted champagne bottle"), absent fever or leukocytosis;

improves with elevation; responds to compression therapy.

• ─────────────────────────────────────────────────────────────────────────────
• Deep Vein Thrombosis Unilateral calf pain and asymmetric edema; lacking bright
• (DVT) superficial warmth and advancing erythema border;

diagnosed via Wells score + D-dimer / duplex ultrasound.

• ─────────────────────────────────────────────────────────────────────────────
• NECROTIZING PAIN OUT OF PROPORTION to physical findings, rapid spread,
• FASCIITIS crepitus (gas), bullae (especially hemorrhagic), skin
• (SURGICAL EMERGENCY!) necrosis/anesthesia, severe systemic toxicity, hypotension;

EMERGENT SURGICAL DEBRIDEMENT + broad-spectrum IV antibiotics.

Caution

RED FLAG CLINICAL WARNING: NECROTIZING FASCIITIS Necrotizing soft tissue infection (NSTI / necrotizing fasciitis) is a rapidly fatal surgical emergency involving the deep muscular fascia and subcutaneous fat. It may initially resemble benign cellulitis, but rapid progression occurs within hours. Hallmark warning signs include:

• Excruciating pain out of proportion to physical examination findings;
• Failure to respond to standard broad-spectrum antibiotics within 12 to 24 hours;

"Hard" physical signs: cutaneous anesthesia (due to thrombosis of cutaneous microvessels and necrosis of dermal sensory nerves), tense wooden edema extending beyond erythema, subcutaneous crepitus (gas in soft tissues), bullae (particularly violaceous or hemorrhagic bullae), and frank skin ecchymosis or gangrene;

Systemic toxicity: high fever, refractory hypotension, tachycardia out of proportion to fever, tachypnea, altered mental status, and marked leukocytosis with bandemia (LRINEC score ≥6);

Immediate Management : DO NOT DELAY SURGICAL EXPLORATION FOR IMAGING! Urgent operative debridement with direct visualization of "dishwater pus" and lack of fascial resistance to probing is both diagnostic and life-saving. Empiric medical resuscitation requires broad-spectrum IV antimicrobials: IV Vancomycin (for MRSA) + IV Piperacillin-tazobactam (for Gram-negative bacilli and anaerobes) + IV Clindamycin (inhibits bacterial ribosome synthesis, shutting down streptococcal pyrogenic exotoxin A/B and staphylococcal toxic shock syndrome toxin synthesis).

Purulent Skin Infections: Folliculitis, Furuncles, Carbuncles & Cutaneous Abscesses

Purulent SSTIs are overwhelmingly caused by Staphylococcus aureus , with Community-Associated MRSA (CA-MRSA) accounting for the majority of purulent skin infections presenting to ambulatory clinics and emergency departments across North America.

Spectrum of Purulent Pathologies

Folliculitis : Superficial bacterial infection localized strictly to the hair follicle ostium. Presents as tiny, 1 to 2 mm, erythematous papules or central pustules pierced by a hair shaft. Typically self-limiting; managed with warm compresses and topical mupirocin 2% or topical clindamycin 1% lotion. Hot tub folliculitis is caused by Pseudomonas aeruginosa (contaminated whirlpools/hot tubs), presenting with pruritic, tender papulopustules in bathing-suit distribution, resolving spontaneously in 7-10 days.

Furuncle ("Boil") : A deep, tender, inflammatory, circumscribed nodule centered on a hair follicle that extends into the deep dermis and subcutaneous tissue, terminating in central necrosis and purulence. Often arises from pre-existing folliculitis.

Carbuncle : A coalescence of multiple neighboring furuncles into a single, large, deeply indurated, extremely painful inflammatory mass. Features multiple loculations and draining follicular orifices ("sieve-like" draining sinus tracts). Commonly located on the posterior neck, upper back, or thighs, and frequently accompanied by systemic symptoms (fever, chills, leukocytosis).

Cutaneous Abscess : A localized collection of pus within the dermis and deeper subcutaneous tissue, presenting as an erythematous, warm, exquisitely tender, fluctuant mass, frequently with a surrounding rim of erythematous induration.

CA-MRSA Virulence & The "Spider Bite" Fallacy

CA-MRSA isolates (predominantly the USA300 pulsotype , carrying the staphylococcal cassette chromosome mec [SCC mec ] type IV or V element) carry specific virulence determinants, notably the Panton-Valentine leukocidin (PVL) gene.

PVL is a pore-forming bicomponent cytotoxin that targets human polymorphonuclear leukocytes and monocytes, causing rapid leukocyte necrosis, deep tissue destruction, and profound inflammatory purulence.

Classic Board & Clinical Pearl : Patients with acute, necrotizing, purulent furuncles or abscesses frequently present insisting they were " bitten by a spider ." In non-endemic areas (outside brown recluse spider habitats in the south-central US), virtually all acute necrotic "spider bites" are CA-MRSA cutaneous abscesses .

Definitive Abscess Management: The Incision & Drainage Standard CUTANEOUS ABSCESS MANAGEMENT ALGORITHM

• Patient Presents with Fluctuant, Tender, Erythematous Subcutaneous Mass
• │
• ▼
• PRIMARY DEFINITIVE THERAPY: INCISION & DRAINAGE (I&D)
• Adequate local anesthesia (field block / freezing spray)
• Linear incision along skin tension lines (Langer lines)
• Blunt breakdown of internal loculations with hemostat
• Copious normal saline irrigation; loose wick if >3-5 cm
• │
• ▼

ARE ADJUNCTIVE ORAL ANTIBIOTICS INDICATED?

Assess for specific high-risk criteria:

• [1] Surrounding cellulitis extending >2 cm from edge
• [2] Systemic signs (T >38°C, HR >90, tachypnea, WBC >12k)
• [3] Multiple abscesses or multiloculated complex collection
• [4] Immunocompromised host (poorly controlled DM, HIV, chemo)
• [5] Extremes of age (infants <6 months, frail elderly)
• [6] High-risk sites (face/danger triangle, hands, genitalia)
• [7] Failure of prior drainage alone
• ╱ ╲
• NO YES
• ╱ ╲
• ▼ ▼

NO ORAL ANTIBIOTICS REQUIRED ADD EMPIRIC ORAL MRSA REGIMEN:

• Warm compresses • TMP-SMX (1-2 DS tabs BID) OR
• Follow-up in 48 hours • Doxycycline (100 mg BID) OR
• Wound checks & dressing change • Clindamycin (300-450 mg TID; D-test)
• Duration: 5 to 7 days
• Antibiotic Stewardship in Simple Abscesses

The Rule : For simple, isolated, uncomplicated cutaneous abscesses successfully drained in immunocompetent patients, routine adjunctive oral antibiotics are NOT indicated and provide no clinically meaningful benefit in cure rates or recurrence prevention!

Evidence : Multiple landmark randomized controlled trials have confirmed that complete mechanical evacuation of pus and disruption of loculations is the definitive curative intervention.

Indications for Adjunctive Oral Antibiotics Post-I&D :

Extensive surrounding cellulitis extending >2 cm beyond the abscess perimeter;

Systemic inflammatory response syndrome (SIRS) : Oral temperature >38.0°C (100.4°F), resting heart rate >90 beats/min, respiratory rate >20 breaths/min, or abnormal white blood cell count (>12,000/mcL or >10% bands);

Multiple abscesses or extensive multiloculated collections;

Immunocompromised host : Poorly controlled diabetes mellitus, active chemotherapy, organ transplantation, advanced HIV/AIDS, or chronic systemic immunosuppressive medications;

Extremes of age : Neonates and infants <6 months of age, or frail elderly patients;

Critical / High-Risk Anatomical Locations :

Central face ("Danger triangle of the face") : Bounded by the corners of the mouth and the nasal bridge; venous drainage via facial and angular veins communicates directly with the ophthalmic veins and the cavernous sinus , creating high risk for septic cavernous sinus thrombosis;

• Hands and digits : Risk of purulent tenosynovitis and fascial space infection;
• Perineum and genitalia : Risk of Fournier gangrene;

Lack of clinical response or rapid recurrence following initial incision and drainage alone.

Empiric Outpatient Oral Antibiotic Regimens for CA-MRSA

Trimethoprim-Sulfamethoxazole (TMP-SMX) :

Dose : 1 to 2 Double-Strength (DS: 160 mg TMP / 800 mg SMX) tablets PO BID for 5 to 7 days .

Spectrum : Outstanding activity against CA-MRSA (>95% susceptibility).

Important Limitation : Poor, unreliable activity against Group A Streptococcus ! If an abscess is accompanied by significant surrounding non-purulent cellulitis (where streptococcal co-infection is suspected), TMP-SMX must be combined with a beta-lactam such as Cephalexin 500 mg PO QID .

Adverse Effects & Precautions : Sulfa allergy, hyperkalemia (especially with concurrent ACE inhibitors/ARBs), acute kidney injury, bone marrow suppression, hemolysis in G6PD deficiency, and severe dermatologic reactions (Stevens-Johnson syndrome). Contraindicated in pregnancy at term (kernicterus) and infants <2 months.

Doxycycline :

Dose : 100 mg PO BID for 5 to 7 days .

Spectrum : Excellent activity against CA-MRSA; limited/variable streptococcal activity.

Precautions : Contraindicated in pregnancy (second and third trimesters; bone/tooth dysgenesis) and breastfeeding; pill-induced esophagitis (must take with a full glass of water and remain upright for 30 minutes); phototoxicity.

Clindamycin :

Dose : 300 mg to 450 mg PO TID for 5 to 7 days .

Spectrum : Unique advantage of providing monotherapy coverage against both CA-MRSA and Streptococcus pyogenes , plus potent inhibition of staphylococcal toxin synthesis (PVL and TSST-1).

The D-Test (Double-Disk Diffusion) : In staphylococcal isolates that test resistant to erythromycin but susceptible to clindamycin , an inducible erm gene (erythromycin ribosome methylase) may mediate resistance under clindamycin exposure. A positive D-test indicates inducible clindamycin resistance , rendering clindamycin ineffective in vivo . Clindamycin should only be used if the D-test is negative.

Major Risk : Potent risk factor for Clostridioides difficile colitis.

Recurrent Furunculosis / CA-MRSA Decolonization Protocol

Patients presenting with recurrent furuncles or abscesses (defined as ≥2 episodes within 6 months) often harbor persistent staphylococcal colonization in mucosal and cutaneous reservoirs (anterior nares, axillae, groin, perineum). Once active infections have resolved, an evidence-based decolonization regimen should be implemented:

Intranasal Mupirocin : Apply mupirocin 2% nasal ointment to both anterior nares twice daily for 5 consecutive days .

Chlorhexidine Body Washes : Daily full-body washing with chlorhexidine gluconate 4% solution from the neck down (leave on skin for 2 minutes before rinsing) for 5 to 14 days .

Environmental & Household Measures : Decontaminate personal hygiene items; do not share towels, washcloths, or razors; launder all sheets, towels, and undergarments in hot water (>60°C / 140°F) with detergent and tumble dry on high heat; evaluate and simultaneously decolonize symptomatic household contacts.

Loading diagram... Clinical Decision and Treatment Algorithm for Bacterial Skin Infections